Three patients with hematologic relapse after bone marrow transplantation for chronic myelogenous leukemia were treated with interferon alpha and transfusion of viable donor buffy coat. All had complete hematologic and cytogenetic remission, which persisted 32 to 91 weeks after treatment. In two patients graft-versus-host disease developed and was treated by immunosuppression. These results are an example of adoptive immunotherapy without cytoreductive chemotherapy or radiotherapy in human chimeras.

Severe microangiopathy has been reported as a rare complication of cyclosporine A (CsA) prophylaxis in allogeneic bone marrow transplantation (BMT). We found morphological and biochemical changes indicative of generalized endothelial damage in 49 of 66 allogeneic marrow graft recipients receiving cyclosporine, but none in 11 patients treated with methotrexate for prophylaxis of graft-v-host disease (GVHD). Changes occurred after engraftment of bone marrow and consisted of intravascular hemolysis with red cell fragmentation and de novo thrombocytopenia. They were preceded by a decrease in activated partial thromboplastin time and fibrinogen indicating activation of coagulation. Endothelial damage as the central lesion of microangiopathy was confirmed by a simultaneous increase of factor VIII related antigen. Severe microangiopathy was observed in ten patients and was fatal in seven. Risk factor analysis revealed a highly significant association of microangiopathy with severity of acute GVHD (aGVHD) (P less than .001) and use of CsA prophylaxis (P less than .001). Our data suggest endothelial damage as a result of cellular activation and subsequent release of cytokines in the course of a aGVHD, which is not inhibited by CsA prophylaxis.

Three patients with hematologic relapse after bone marrow transplantation for chronic myelogenous leukemia were treated with interferon alpha and transfusion of viable donor buffy coat. All had complete hematologic and cytogenetic remission, which persisted 32 to 91 weeks after treatment. In two patients graft-versus-host disease developed and was treated by immunosuppression. These results are an example of adoptive immunotherapy without cytoreductive chemotherapy or radiotherapy in human chimeras.

Platelet aggregation studies generally are performed in platelet-rich plasma (PRP) by the turbidometric method. The authors compared this technic with the recently introduced impedance aggregometry in PRP and whole blood (WB). In healthy controls there was a good correlation between the two technics when aggregation was induced by ADP or collagen. As compared with PRP, platelets in WB were more sensitive to the aggregating effect of thrombin, ristocetin, and arachidonic acid. Platelet sensitivity to prostacyclin was increased in WB. The anti-platelet effect of a single oral dose of aspirin could be detected for a longer period in WB than in PRP. Platelet aggregation tests in WB from patients with platelet dysfunctions showed the same response pattern to different aggregating agents as in PRP. In contrast to turbidometry, the impedance method in PRP and WB enabled registration of platelet aggregation in a dose-dependent fashion in a sample from a patient with severe hyperlipoproteinemia. It is concluded that platelet aggregation can be studied conveniently with the impedance method in the more physiologic medium of WB. Providing the same information as the well-established turbidometry, the time-sparing impedance method needs less citrated blood. Moreover, our results show an increased sensitivity of the WB system to some aggregating and anti-platelet agents.

C57BL/6 mice or pure cultures of their macrophages were inoculated with Newcastle disease virus (NDV) or poly(I).poly(C) to induce interferons (IFNs) that were separated on CH-Sepharose 4B columns. The elution profiles of different activity peaks were compared. All preparations induced in vivo showed the same pattern but the relative proportions of the IFN activities varied. In vitro poly(I).poly(C)-induced IFN showed two peaks after separation by the column, and three peaks were found when NDV-induced IFNs were separated. When IFN induced by NDV in vitro was used to determine the molecular weight, activities were observed in three molecular weight ranges. The smallest one with 18,000 daltons was neutralized by anti-IFN-alpha and represented about 7% of the total activity. The activities of molecular weights 24,000 daltons and 29,000-31,000 daltons were neutralized by anti-IFN-beta. Poly(I).poly(C)-induced IFN in vitro showed two molecular weight ranges, 26,000 daltons and 40,000 daltons, and both were neutralized by anti-IFN-beta. IFN induced in serum by NDV at 3 h had molecular weights of 18,000 daltons neutralized by anti-IFN-alpha and 26,000-30,000 daltons neutralized by anti-IFN-beta. Both IFN subtypes were represented at equal quantities. Serum IFN found in the serum after 8 h had three molecular weight ranges: 18,500-19,500 daltons neutralized by anti-IFN-alpha containing 80% of the total IFN amount, 26,000-27,000 daltons, and 38,000 daltons both neutralized by anti-IFN-beta and containing 20% of the IFN.(ABSTRACT TRUNCATED AT 250 WORDS)